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Papel del homólogo p53 p73 en la apoptosis inducida por E2F-1
M Irwin1, M C Marin, A C Phillips
1Dana-Farber Cancer Institute and Brigham and Womens Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Nature
|October 18, 2000
Resumen
El factor de transcripción E2F-1 desencadena la muerte celular a través de rutas dependientes e independientes de p53. Este estudio revela que E2F-1 activa p73, un homólogo de p53, para inducir la apoptosis incluso cuando p53 está ausente.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Biología celular Biología celular.
- Investigación de Investigación del Cáncer.
Sus antecedentes:
- El factor de transcripción E2F-1 juega un doble papel en la progresión del ciclo celular y la apoptosis.
- E2F-1 utiliza ambas vías p53-dependiente y p53-independiente para inducir la muerte celular.
- La vía dependiente de p53 implica que E2F-1 induzca p14ARF, que neutraliza el HDM2 y estabiliza el p53.
Objetivo del estudio:
- Para investigar el papel del homólogo p53 p73 en la apoptosis inducida por E2F-1.
- Para determinar si E2F-1 puede inducir la apoptosis a través de p73 en ausencia de p53.3 funcional.
Principales métodos:
- Análisis del efecto de E2F-1 en la transcripción de p73.
- Evaluación de la apoptosis inducida por E2F-1 en células con alteración de la función p73.
- Experimentos realizados en células tumorales p53-defectuosas y fibroblastos de embriones de ratón p53-/- .
Principales resultados:
- Se demostró que E2F-1 induce la transcripción de p73.
- La alteración de la función p73 inhibió significativamente la apoptosis inducida por E2F-1.
- Esta inhibición se observó tanto en las células tumorales p53-defectuosas como en los fibroblastos de embriones de ratón p53-/- .
Conclusiones:
- La activación de p73 es un mecanismo por el cual E2F-1 puede inducir la apoptosis.
- E2F-1 puede desencadenar la muerte celular a través de p73 incluso en ausencia de p53.
- Este hallazgo pone de relieve la importancia de la vía p73 en las respuestas celulares mediadas por E2F-1.
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